Chapter 13. Memory, Learning, and Development

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 81 - 100 of 5818

Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.

Keyword: Alzheimers; Language
Link ID: 23259 - Posted: 02.21.2017

By WINNIE HU Ruth Brunn finally said yes to marijuana. She is 98. She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb. “I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.” Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own. From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects. For some people, it is a last resort when nothing else helps. Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease. © 2017 The New York Times Company

Keyword: Drug Abuse; Alzheimers
Link ID: 23255 - Posted: 02.20.2017

By JANE E. BRODY “Feeling My Way Into Blindness,” an essay published in The New York Times in November by Edward Hoagland, an 84-year-old nature and travel writer and novelist, expressed common fears about the effects of vision loss on quality of life. Mr. Hoagland, who became blind about four years ago, projected deep-seated sadness in describing the challenges he faces of pouring coffee, not missing the toilet, locating a phone number, finding the food on his plate, and knowing to whom he is speaking, not to mention shopping and traveling, when he often must depend on the kindness of strangers. And, of course, he sorely misses nature’s inspiring vistas and inhabitants that fueled his writing, though he can still hear birds chatter in the trees, leaves rustle in the wind and waves crash on the shore. Mr. Hoagland is hardly alone in his distress. According to Action for Blind People, a British support organization, those who have lost some or all sight “struggle with a range of emotions — from shock, anger, sadness and frustration to depression and grief.” When eyesight fails, some people become socially disengaged, leading to isolation and loneliness. Anxiety about a host of issues — falls, medication errors, loss of employment, social blunders — is common. A recent study from researchers at the Wilmer Eye Institute at Johns Hopkins University School of Medicine found that most Americans regard loss of eyesight as the worst ailment that could happen to them, surpassing such conditions as loss of limb, memory, hearing or speech, or having H.I.V./AIDS. Indeed, low vision ranks behind arthritis and heart disease as the third most common chronic cause of impaired functioning in people over 70, Dr. Eric A. Rosenberg of Weill Cornell Medical College and Laura C. Sperazza, a New York optometrist, wrote in American Family Physician. © 2017 The New York Times Company

Keyword: Vision; Development of the Brain
Link ID: 23253 - Posted: 02.20.2017

Bret Stetka In a series of recent interviews, President Donald Trump's longtime personal physician Dr. Harold N. Bornstein told The New York Times that our new commander in chief has what amounts to a pretty unremarkable medical chart. Like about a quarter of American adults, Trump is on a statin for high cholesterol. He also takes a daily baby aspirin for heart health, an occasional antibiotic for rosacea, a skin condition, and Propecia, a pill to promote hair growth. Bornstein also told the Times that should he be appointed White House doctor, he probably wouldn't test the president for baseline dementia risk, something many doctors have argued should be mandatory. At 70, Trump is the oldest American president to ever take office. Couple his age with a family history of dementia — his father Fred developed Alzheimer's disease in his 80s — and one could argue that the question of baseline cognitive testing for the U.S. head of state has taken on new relevance. An assortment of fairly simple tests exist that can establish a reference point for cognitive capacity and detect early symptoms of mental decline. One of the most common such screens is the Mini-Mental Status Examination, a series of questions that gauges attention, orientation and short-term memory. It takes about five to 10 minutes to complete. Yet admitting vulnerability of any kind isn't something politicians have been keen to do. The true health of politicians has likely been cloaked in secrecy since the days of Mesopotamian kings, but definitely since the Wilson administration. © 2017 npr

Keyword: Alzheimers
Link ID: 23243 - Posted: 02.17.2017

Ewen Callaway Researchers have no way to tell whether young babies may later be diagnosed with autism. But brain scans could help, a small study suggests. By scanning the brains of babies whose siblings have autism, researchers say they have been able to make reasonably accurate forecasts about which of these high-risk infants will later develop autism themselves. The findings raise the prospect of diagnosing autism spectrum disorder (ASD) months before children develop symptoms, a goal that has proved elusive. Nature looks at the new study and its implications. Why has it been so tough to diagnose autism in infants? Children typically show symptoms of ASD, such as difficulty making eye contact, after the age of 2. Researchers believe that the brain changes underlying ASD begin much earlier — possibly even in the womb. But behavioural assessments haven't been helpful in predicting who will get autism, says Joseph Piven, a psychiatrist at the University of North Carolina (UNC) in Chapel Hill, who co-led the study, published online in Nature1. “Children who end up with autism at 2 or 3, they don’t look like they have autism in the first year," he says. Certain rare mutations are linked to ASD, but the vast majority of cases cannot be pinned to a single or even a handful of genetic risk factors. Beginning in the 1990s, Piven and other researchers noticed that children with autism tended to have larger brains than developmentally normal children, suggesting that brain growth could be a biomarker for ASD. But Piven and colleague Heather Cody Hazlett, a psychologist at UNC-Chapel Hill, say it had not been clear when overgrowth occurred. What did their latest study look at? © 2017 Macmillan Publishers Limited,

Keyword: Autism; Brain imaging
Link ID: 23240 - Posted: 02.16.2017

By Amy Ellis Nutt For the first time, scientists can point to substantial empirical evidence that people with attention-deficit/hyperactivity disorder have brain structures that differ from those of people without ADHD. The common disorder, they conclude, should be considered a problem of delayed brain maturation and not, as it is often portrayed, a problem of motivation or parenting. In conducting the largest brain imaging study of its kind, an international team of researchers found that ADHD involves decreased volume in key brain regions, in particular the amygdala, which is responsible for regulating the emotions. Although the study, published Wednesday in the Lancet Psychiatry, included children, adolescents and adults, the scientists said the greatest differences in brain volume appeared in the brains of children. Of seven subcortical brain regions targeted in the study, five, including the amygdala, were found to be smaller in those with ADHD, compared with those in a control group. The other regions that showed reductions in volume were: the caudate nucleus (which has been linked to goal-directed action), the putamen (involved in learning and responding to stimuli), the nucleus accumbens (which processes rewards and motivation) and the hippocampus (where memories are formed). © 1996-2017 The Washington Post

Keyword: ADHD; Development of the Brain
Link ID: 23239 - Posted: 02.16.2017

By John Carroll, Scratch yet another Phase III Alzheimer’s drug hopeful. Merck announced late Tuesday that it is shuttering its EPOCH trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues. This is one of Merck’s top late-stage drugs, and news of the failure drove down the pharma giant’s shares in after-market trading by 2.45%. BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab — which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down. Merck’s effort was the most advanced in the pipeline, but Eli Lilly and others are still in hot pursuit with their own persistent BACE efforts. Teams from Biogen/Eisai and Novartis/Amgen are also beavering away on BACE. “Alzheimer’s disease is one of the most pressing and daunting medical issues of our time, with inherent, substantial challenges to developing an effective disease-modifying therapy for people with mild-to-moderate disease. Studies such as EPOCH are critical, and we are indebted to the patients in this study and their caregivers,” said Dr. Roger M. Perlmutter, president, Merck Research Laboratories. © 2017 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 23238 - Posted: 02.16.2017

By Jesse Singal Those who advocate for sound, evidence-based research about autism are extremely alarmed about Donald Trump, and for good reason: In addition to Trump’s ties to Andrew Wakefield, the disgraced British doctor whose debunked research helped fuel the false idea of links between childhood vaccines and autism, Robert F. Kennedy Jr., a notorious anti-vaxxer himself, told reporters back in January that Trump planned to tap him as chair of a commission on “vaccine safety.” There is no question at this point that Trump has significant connections to a pseudoscientific medical movement that spreads dangerous, disproven ideas. Today, Trump gave nervous observers yet more reason to worry. It occurred at a White House event in which Trump and Secretary of Education Betsy DeVos met with a bunch of educators. Trump seemed to fixate, for a moment, on one educator named Jane (her last name is hard to make out) after she explained that she is the principal of a special education center in Virginia. The sequence starts at about 5:38 in this video: After Jane noted that many of her students have autism, Trump asked, “Have you seen a big increase in the autism, with the children?” Jane replied in the affirmative, but seemed to couch her response as being more about an increase in demand for services — she didn’t explicitly agree there’s been a big increase in the overall rate. Trump continued: “So what’s going on with autism? When you look at the tremendous increase, it’s really — it’s such an incredible — it’s really a horrible thing to watch, the tremendous amount of increase. Do you have any idea? And you’re seeing it in the school?” Jane replied — again, in a way that seems a bit noncommittal vis-à-vis Trump’s claim — that the rate of autism is something like 1-in-66 or 1-in-68 children. To which Trump responds: “Well now, it’s gotta be even lower [presumably meaning higher, rate-wise] than that, which is just amazing — well, maybe we can do something.” (Jane had the rate right, and Trump is incorrect that it has crept higher.) © 2017, New York Media LLC.

Keyword: Autism
Link ID: 23233 - Posted: 02.15.2017

Jon Hamilton Researchers have created mice that appear impervious to the lure of cocaine. Even after the genetically engineered animals were given the drug repeatedly, they did not appear to crave it the way typical mice do, a team reports in Nature Neuroscience. "They didn't keep going into the room where they received the cocaine and they seemed to be just as happy exploring all around the cage," says Shernaz Bamji, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia in Vancouver. "Addiction is a form of learning," Bamji says. And somehow, these mice never learned to associate the pleasurable feelings produced by cocaine with the place where they received the drug. The result was startling because the scientists thought these mice would be especially susceptible to addiction. "We repeated the experiment several times to see if we had made a mistake," Bamji says. The reason for the team's surprise had to do with proteins that affect learning. The animals had been genetically engineered to produce high levels of proteins called cadherins in the brain's "reward circuit," which plays an important role in addiction. And genetic studies have suggested that people with high levels of cadherins are more susceptible to drug addiction. Cadherins act a bit like glue, binding cells together. Usually this glue enhances learning by strengthening the connections, or synapses, between brain cells. © 2017 npr

Keyword: Drug Abuse; Learning & Memory
Link ID: 23228 - Posted: 02.14.2017

Ian Sample Science editor Children who are born very prematurely are at greater risk of developing mental health and social problems that can persist well into adulthood, according to one of the largest reviews of evidence. Those with an extremely low birth weight, at less than a kilogram, are more likely to have attention disorders and social difficulties as children, and feel more shyness, anxiety and depression as adults, than those born a healthy weight. The review draws on findings from 41 published studies over the past 26 years and highlights the need for doctors to follow closely how children born very prematurely fare as they become teenagers and adults. “It is important that families and doctors be aware of the potential for these early-emerging mental health problems in children born at extremely low birth weight, since at least some of them endure into adulthood,” said Karen Mathewson, a psychologist at McMaster University in Ontario. Improvements in neonatal care in the past two decades mean that more children who are born very prematurely now survive. In a healthy pregnancy, a baby can reach 1kg (a little more than 2lbs) within 27 weeks, or the end of the second trimester. The study, which involves data from 13,000 children in 12 different countries, follows previous research that found a greater tendency for very low birth weight children to have lower IQs and autism and more trouble with relationships and careers as they reach adulthood and venture into the world. © 2017 Guardian News and Media Limited

Keyword: Development of the Brain; ADHD
Link ID: 23227 - Posted: 02.14.2017

After A Stroke At 33, A Writer Relies On Journals To Piece Together Her Own Story On New Year's Eve, 2006, Christine Hyung-Oak Lee developed a splitting headache. She was 33, and her world turned upside down — as in, she literally saw the world upside down. Suddenly, she could hold things in her mind for only 15 minutes at a time. She was a writer who now couldn't recall words or craft sentences. She remembers looking at the phone and thinking to herself: What is the phone number for 911? Days later, she learned she'd had a stroke. "I had a 15-minute short-term memory, like Dory the fish in Finding Nemo," Lee wrote in a Buzzfeed essay chronicling her experience. "My doctors instructed me to log happenings with timestamps in my Moleskine journal. That, they said, would be my working short-term memory. My memento to my mori." Lee used those journals to reconstruct her experience in a new memoir called Tell Me Everything You Don't Remember. She talks with NPR's Scott Simon about the silver linings of memory loss and the unexpected grief that came with her recovery. Interview Highlights On what it's like to have a 15-minute memory You don't even fathom the magnitude of your loss — or at least I didn't. I couldn't plan for the future. I couldn't think of the past. I had no regrets. So it's literally living in the moment. I was experiencing something that people go to yoga and Zen retreats to achieve. So it was quite pleasant. It was not pleasant for the people around me. But in that period of my recovery, where I couldn't remember everything, I think I was incredibly at peace and happy. On having an "invisible" disability It was frustrating. On the one hand, you want people to know: Hey, slow down for me. Hey, I'm going through a crisis. On the other hand, I was also privileged to be disabled in a way that wasn't visible. So people also didn't treat me any differently. So it was very isolating. ... When I told people that I was sick and I needed them to slow down, along with that came this need to explain my position and I ... felt a lot of resentment for having to do with that. © 2017 npr

Keyword: Stroke; Learning & Memory
Link ID: 23213 - Posted: 02.11.2017

Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,

Keyword: Regeneration; Stem Cells
Link ID: 23210 - Posted: 02.10.2017

“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.

Keyword: Epilepsy; Development of the Brain
Link ID: 23209 - Posted: 02.10.2017

In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.

Keyword: Alzheimers
Link ID: 23205 - Posted: 02.09.2017

By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist

Keyword: Drug Abuse; Learning & Memory
Link ID: 23203 - Posted: 02.09.2017

by Linda Rodriguez McRobbie If you ask Jill Price to remember any day of her life, she can come up with an answer in a heartbeat. What was she doing on 29 August 1980? “It was a Friday, I went to Palm Springs with my friends, twins, Nina and Michelle, and their family for Labour Day weekend,” she says. “And before we went to Palm Springs, we went to get them bikini waxes. They were screaming through the whole thing.” Price was 14 years and eight months old. What about the third time she drove a car? “The third time I drove a car was January 10 1981. Saturday. Teen Auto. That’s where we used to get our driving lessons from.” She was 15 years and two weeks old. The first time she heard the Rick Springfield song Jessie’s Girl? “March 7 1981.” She was driving in a car with her mother, who was yelling at her. She was 16 years and two months old. Price was born on 30 December 1965 in New York City. Her first clear memories start from around the age of 18 months. Back then, she lived with her parents in an apartment across the street from Roosevelt Hospital in Midtown Manhattan. She remembers the screaming ambulances and traffic, how she used to love climbing on the living room couch and staring out of the window down 9th Avenue. When she was five years and three months old, her family – her father, a talent agent with William Morris who counted Ray Charles among his clients; her mother, a former variety show dancer, and her baby brother – moved to South Orange, New Jersey. They lived in a three-storey, red brick colonial house with a big backyard and huge trees, the kind of place people left the city for. Jill loved it.

Keyword: Learning & Memory
Link ID: 23201 - Posted: 02.08.2017

By Julia Shaw We all have times of day when we are not at our best. For me, before 10am, and between 2-4pm, it’s as though my brain just doesn’t work the way it should. I labor to come up with names, struggle to keep my train of thought, and my eloquence drops to the level expected of an eight-year-old. In an effort to blame my brain for this, rather than my motivation, I reached out to a researcher in the area of sleep and circadian neuroscience. Andrea Smit, a PhD student working with Professors John McDonald and Ralph Mistlberger at Simon Fraser University in Canada, was happy to help me find excuses for why my memory is so terribly unreliable at certain times of day. Humans have daily biological rhythms, called circadian rhythms, which affect almost everything that we do. They inform our bodies when it is time to eat and sleep, and they dictate our ability to remember things. According to Smit, “Chronotype, the degree to which someone is a “morning lark” or a “night owl,” is a manifestation of circadian rhythms. In a recent study, Smit used EEG, a type of brain scan, to study the interaction between chronotypes and memory. “Testing extreme chronotypes at multiple times of day allowed us to compare attentional abilities and visual short term memory between morning larks and night owls. Night owls were worse at suppressing distracting visual information and had a worse visual short term memory in the morning as compared with the afternoon,” she says. “Our research shows that circadian rhythms interact with memories even at very early stages of processing within the brain.” © 2017 Scientific American

Keyword: Biological Rhythms; Learning & Memory
Link ID: 23194 - Posted: 02.07.2017

By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 23190 - Posted: 02.06.2017

Diana Steele Generations of gurus have exhorted, “Live in the moment!” For Lonni Sue Johnson, that’s all she can do. In 2007, viral encephalitis destroyed Johnson’s hippocampus. Without that crucial brain structure, Johnson lost most of her memories of the past and can’t form new ones. She literally lives in the present. In The Perpetual Now, science journalist Michael Lemonick describes Johnson’s world and tells the story of her life before her illness, in which she was an illustrator (she produced many New Yorker covers), private pilot and accomplished amateur violist. Johnson can’t remember biographical details of her own life, recall anything about history or remember anything new. But remarkably, she can converse expertly about making art and she creates elaborately illustrated word-search puzzles. She still plays viola with expertise and expression and, though she will never remember that she has seen it before, she can even learn new music. Neuroscientists are curious about Johnson’s brain in part because her education and expertise before her illness contrast sharply with that of the most famous amnesiac known to science, Henry Molaison. Lemonick interweaves the story of “Patient H.M.,” as he was known, with Johnson’s biography. Molaison had experienced seizures since childhood and held menial jobs until surgery in his 20s destroyed his hippo-campus. At the time, in the 1950s, Molaison’s subsequent amnesia came as a surprise, prompting a 50-year study of his brain that provided a fundamental understanding of the central role of the hippocampus in forming conscious memories. © Society for Science & the Public 2000 - 2016.

Keyword: Learning & Memory
Link ID: 23189 - Posted: 02.06.2017

Hannah Devlin Science correspondent It sounds like torment for the smoker attempting to quit: handling packets of cigarettes and watching footage of people smoking, without being allowed to light up. However, scientists believe that lengthy exposure to environmental triggers for cravings could be precisely what smokers need to help them quit. The technique, known as extinction therapy, targets the harmful Pavlovian associations that drive addiction with the aim of rapidly “unlearning” them. The latest study, by scientists at the Medical University of South Carolina, found that after two one-hour sessions people smoked significantly fewer cigarettes one month after treatment compared to a control group. The study was not an unqualified success – many participants still relapsed after treatment – but the authors believe the work could pave the way for new approaches to treating addiction. Michael Saladin, the psychologist who led the work, said: “When I initially saw the results from this study it was pretty eye-opening.” In smokers, environmental triggers have typically been reinforced thousands of times so that the sight of a lighter, for instance, becomes inextricably linked to the rush of nicotine that the brain has learned will shortly follow. After quitting an addictive substance, these associations fade slowly over time, but people often flounder in the first days and weeks when cravings are most powerful. Saladin and others believe it is possible to fast-track this process in carefully designed training sessions, to help people over the initial hurdle. © 2017 Guardian News and Media Limited

Keyword: Drug Abuse; Learning & Memory
Link ID: 23187 - Posted: 02.04.2017